Clinical Relevance
Our study included a relatively large cohort of AF ablation patients with a unique characteristic – the use of amiodarone in the pre-ablation period for purposes of rhythm control. We were able to use this substantial cohort of amio-treated patients to investigate whether therapeutic response to the drug predicted ablation outcomes with standard ablation approaches (a predominantly PVI-based strategy; irrigated, force-sensing RF or second-generation cryoballoon cathters).
Previous studies of AAD use before AF ablation have focused on three main ideas: response to AADs as a test to predict ablation outcome; AAD maintenance of sinus rhythm to allow atrial reverse remodeling prior to ablation; and AAD therapy to minimize non-PV foci targeted during the ablation procedure.
Miyazaki and colleagues analyzed the relationship between pre-ablation response to bepridil (a calcium-blocking anti-anginal) and ablation outcomes in 82 patients with persAF exclusively (7). Their study found that post-ablation AF freedom was greater in the patients who cardioverted pharmacologically with the bepridil (no electrical cardioversion performed) than in the patients who did not cardiovert with bepridil therapy. Kang and colleagues conducted an analogous study investigating pre-ablation electrical cardioversion efficacy in AF patients. They found that those persAF patients (94) who were more easily cardioverted pre-ablation (lower energy; fewer shocks) had improved ablation outcomes as compared to patients who were more difficult to cardiovert (11).
Our study tests a similar idea to the one investigated by Miyazaki and Kang: does pre-procedure response to a rhythm-control strategy (AAD or cardioversion) predict response to catheter ablation for AF? Unlike the previous reports mentioned, we found that pre-procedure response to amiodarone was not a reliable predictor of post-ablation outcomes. We were able to study a large cohort of patients relative to these previous reports. All patients were restored to sinus rhythm (unlike the Miyazaki study) prior to ablation, making ours more an investigation of trigger suppression rather than termination of ongoing AF. Finally, and importantly, most of our patients received what many would consider standard therapy for patients with PAF or persAF (PVI only), rather than extensive (and often pro-arrhythmic) supplemental ablation beyond PVI.
A second type of study, focusing on atrial structural and electrical remodeling with AAD therapy to maintain NSR in the pre-ablation window, is supported by pre-clinical investigations of amiodarone on atrial electrophysiology. Amiodarone therapy in canine models of AF prevents action potential shortening, depressed conduction velocity, interstitial fibrosis deposition, and AF inducibility (12,13). Based on that idea of pre-ablation conditioning with amiodarone, Benak and colleagues investigated 62 persAF patients treated with amiodarone and cardioversion three months prior to anticipated PVI (9). They selected the patients who maintained NSR on amiodarone and performed PVI, finding comparable ablation results to a matched cohort of patients with PAF. They did not perform ablation in the group of persAF patients who did not maintain NSR on amiodarone. Our investigation extends the findings of the Benak study, in which patients who failed amiodarone therapy were not allowed to undergo PVI; our results suggest that this group should not have ablation therapy denied them solely because of failure to respond to amiodarone treatment.
Finally, a number of studies have demonstrated that pre-treatment with amiodarone limits the number of non-PV targets seen at the time of ablation, allowing for reduced procedural and ablation times (14,15,16). These investigations used an extensive ablation approach for patients with persAF, with routine lesion application targeting non-PV sites. We believe that the ablation approach in our investigation reflects broad trends in the field of catheter ablation for both persAF and PAF, with an emphasis on PVI and a de-emphasis on the routine application of potentially pro-arrhythmic lesion sets (lines, low-voltage homogenization, etc.) (17).